Table 2.

EGFR mutation and MET status of lung adenocarcinoma cell lines and tumor samples from patients with acquired resistance to EGFR inhibitors

PatientEGFR mutationT790MMET F.C.DrugDuration, months
H820Del E746-E749Y 2.7 NANA
PC-9Del E746-A750N0.8NANA
1Del L747-E749; A750PYnot amp. by aCGHerl.26
2Del L747-P753N 1.8 erl.22
3Del E746-A750N0.6*gef.11
4Del E746-A750Nnot amp. by aCGHgef.9
6Del E746-A750N 1.8*erl.9
7Del E746-T751insAN0.6*erl.10
8Del L747-S752insQNnot amp. by aCGHerl.32
9L858RNnot amp. by aCGHgef., erl.>25
10aDel L747-T751; K754EY 1.8*gef.11
10bDel L747-T751; K754EN 3.5*gef.11
11L858RYnot amp. by aCGHgef.47
12L858RNnot amp. by aCGHgef.15
13L858RYnot amp. by aCGHerl.17
14Del E746-A750Y0.5gef., erl.31
15Del E746-A750N0.8gef., erl.32
16Del E746-A750N0.5erl.24
H820Del E746-E749Y 2.2 NANA
17Del E746-A750Y1.1erl.6
18Del E746-A750N1.1gef.5
19Del E746-A750N 2.8 gef., erl.27
  • EGFR mutation status was determined as described in the Materials and Methods; the absence or presence of the drug-resistance EGFRT790M mutation is indicated by a Y (yes) or N (no). For patient no. 10, two individual samples (10a and 10b) were examined. For MET fold change, values are given relative to MTHFR as assessed by qPCR, described in the Materials and Methods, with DNA from a reference sample (Ref.) and H820 cells included in each set. Samples with MET amplification are in boldface. None of the seven samples for which only aCGH was performed showed MET amplification [″not amplified (amp.) by aCGH″]. Samples for which both qPCR and aCGH were performed are marked with an asterisk. Tumor samples 6, 10a, and 10b all showed focal MET amplification by aCGH (see SI Fig. 4) and by qPCR. Tumor no. 6 also displayed MET amplification by FISH (see text and SI Fig. 5). F.C., fold change; NA, not applicable; Del, deletion; ins; insertion; erl., erlotinib; gef., gefitinib. Time in months patient was on kinase inhibitor treatment when re-biopsy was performed.